Cardiac toxicity from bisphenol A exposure in human-induced pluripotent stem cell-derived cardiomyocytes > REFERENCE LIBRARY

Highlights

BPA exposure changes cardiac field potential in hiPSC-CMs.

BPA exposure affects Cav1.2, Nav1.5 and hERG channel activity.

BPA exposure inhibits Ca²⁺ transients and cardiac contraction in hiPSC-CMs.

Abstract

Bisphenol A (BPA) is a well-known endocrine-disrupting chemical that is widely used in a variety of products, including plastics, medical equipment and receipts. Hence, most people are exposed to BPA through the skin, via inhalation and via the digestive system, and such exposure has been linked to cardiovascular diseases including coronary artery disease, hypertension, atherosclerosis, and myocardial infarction. However, the underlying mechanisms of cardiac dysfunction caused by BPA remain poorly understood. In this study, we found that BPA exposure altered cardiac function in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Acute BPA exposure in hiPSC-CMs resulted in reduced field potential, as measured by multielectrode array (MEA). Furthermore, we observed that BPA dose-dependently inhibited I_Ca, I_Na or I_Kr channels. In addition, BPA exposure dose-dependently inhibited calcium transients and contraction in hiPSC-CMs. Our findings suggest that BPA exposure leads to cardiac dysfunction and cardiac risk factors such as arrhythmia.